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目的探讨L-精氨酸对光气中毒急性肺损伤的治疗作用。方法将48只SD大鼠按随机数字表法分为正常对照组、L-精氨酸对照组、光气中毒组、L-精氨酸低剂量治疗组、L-精氨酸中剂量治疗组、L-精氨酸高剂量治疗组、地塞米松治疗组、L-精氨酸+地塞米松治疗组,每组6只,除正常对照组和L-精氨酸对照组外,其余组动物暴露于0.45 g固体光气发生舱室内,染毒5 min,于染毒后立即腹腔注射L-精氨酸、地塞米松及生理盐水。于染毒后2、4、6 h用小动物肺功能仪测定各组动物的肺功能指标;染毒6 h后处死动物,测定肺组织湿干质量比,血浆还原型谷胱甘肽(reduced glutathione,GSH)、丙二醛(malondialdehyde,MDA)含量,超氧化物岐化酶(superoxide dismutase,SOD)及诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)活力;光学显微镜下观察肺组织病理学变化。结果与正常对照组比较,光气中毒组肺功能指标发生显著变化,肺湿干质量比、血浆MDA含量及iNOS活力显著升高,血浆GSH含量和SOD活力显著下降(P<0.05,P<0.01)。与光气中毒组比较,L-精氨酸各剂量治疗组对光气中毒大鼠肺功能指标有一定改善作用,但差异无统计学意义(P>0.05),肺湿干质量比、血浆MDA含量及iNOS活力显著降低,血浆GSH含量和SOD活力显著升高(P<0.05,P<0.01);地塞米松治疗组血浆MDA含量显著降低,SOD活力显著升高(P<0.05),但肺湿干质量比、血浆GSH含量及iNOS活力无显著变化(P>0.05)。结论 L-精氨酸对光气致肺损伤有保护作用,其机制可能与清除自由基抗氧化及抑制iNOS有关。
Objective To investigate the therapeutic effect of L-arginine on acute lung injury induced by phosgene poisoning. Methods 48 SD rats were randomly divided into normal control group, L-arginine control group, phosgene poisoning group, L-arginine low-dose treatment group, L-arginine medium dose treatment group , L-arginine high-dose treatment group, dexamethasone treatment group, L-arginine + dexamethasone treatment group, 6 in each group, except the normal control group and L-arginine control group, the other group Animals were exposed to 0.45 g solid phosgene generation compartment, exposed to 5 min, immediately after injection of L-arginine, dexamethasone and normal saline. Pulmonary function indexes of each group of animals were determined by using small animal lung function instrument at 2, 4 and 6 hours after exposure. Animals were sacrificed at 6 hours after exposure and the wet / dry weight ratio of lung tissue was measured. Plasma reduced glutathione glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD) and inducible nitric oxide synthase (iNOS) Histopathological changes. Results Compared with the normal control group, the pulmonary function indexes of the phosgene poisoning group changed significantly. The lung wet weight ratio, the content of plasma MDA and the activity of iNOS were significantly increased, while the levels of plasma GSH and SOD were significantly decreased (P <0.05, P <0.01) ). Compared with the phosgene poisoning group, the L-arginine treatment groups had some effects on the lung function of rats with phosgene poisoning, but the difference was not statistically significant (P> 0.05), lung wet-dry mass ratio, plasma MDA (P <0.05, P <0.01). The content of plasma MDA and the activity of iNOS in plasma were significantly decreased (P <0.05, P <0.01) Wet-dry mass ratio, plasma GSH content and iNOS activity had no significant changes (P> 0.05). Conclusion L-arginine has a protective effect on phosgene-induced lung injury. Its mechanism may be related to the anti-oxidation of free radicals and the inhibition of iNOS.